Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-16083
PROVIDER: PRJNA115511 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:OBJECTIVE: To characterize the hormonal milieu and adipose gene expression in response to catch-up growth (CUG), a growth pattern associated with obesity and diabetes risk, in a mouse model of low birth weight (LBW). RESEARCH DESIGN AND METHODS: ICR mice were food restricted by 50% from gestational days 12.5-18.5, reducing offspring birth weight by 25%. During the suckling period, dams were either fed ad libitum, permitting CUG in offspring, or food restricted, preventing CUG. Offspring were killed at age 3 weeks, and gonadal fat was removed for RNA extraction, array analysis, RT-PCR, and evaluation of cell size and number. Serum insulin, thyroxine (T4), corticosterone, and adipokines were measured. RESULTS: At age 3 weeks, LBW mice with CUG (designated U-C) had body weight comparable with controls (designated C-C); weight was reduced by 49% in LBW mice without CUG (designated U-U). Adiposity was altered by postnatal nutrition, with gonadal fat increased by 50% in U-C and decreased by 58% in U-U mice (P < 0.05 vs. C-C mice). Adipose expression of the lipogenic genes Fasn, AccI, Lpin1, and Srebf1 was significantly increased in U-C compared with both C-C and U-U mice (P < 0.05). Mitochondrial DNA copy number was reduced by >50% in U-C versus U-U mice (P = 0.014). Although cell numbers did not differ, mean adipocyte diameter was increased in U-C and reduced in U-U mice (P < 0.01). CONCLUSIONS: CUG results in increased adipose tissue lipogenic gene expression and adipocyte diameter but not increased cellularity, suggesting that catch-up fat is primarily associated with lipogenesis rather than adipogenesis in this murine model. Epididymal fat samples were obtained at age 3 weeks from 5 control mice (CC), 5 mice exposed to in utero undernutrition (UC), and 4 mice exposed to undernutrition in utero and during suckling (UU).
2010-03-04 | E-GEOD-16083 | biostudies-arrayexpress
Project description:OBJECTIVE: To characterize the hormonal milieu and adipose gene expression in response to catch-up growth (CUG), a growth pattern associated with obesity and diabetes risk, in a mouse model of low birth weight (LBW). RESEARCH DESIGN AND METHODS: ICR mice were food restricted by 50% from gestational days 12.5-18.5, reducing offspring birth weight by 25%. During the suckling period, dams were either fed ad libitum, permitting CUG in offspring, or food restricted, preventing CUG. Offspring were killed at age 3 weeks, and gonadal fat was removed for RNA extraction, array analysis, RT-PCR, and evaluation of cell size and number. Serum insulin, thyroxine (T4), corticosterone, and adipokines were measured. RESULTS: At age 3 weeks, LBW mice with CUG (designated U-C) had body weight comparable with controls (designated C-C); weight was reduced by 49% in LBW mice without CUG (designated U-U). Adiposity was altered by postnatal nutrition, with gonadal fat increased by 50% in U-C and decreased by 58% in U-U mice (P < 0.05 vs. C-C mice). Adipose expression of the lipogenic genes Fasn, AccI, Lpin1, and Srebf1 was significantly increased in U-C compared with both C-C and U-U mice (P < 0.05). Mitochondrial DNA copy number was reduced by >50% in U-C versus U-U mice (P = 0.014). Although cell numbers did not differ, mean adipocyte diameter was increased in U-C and reduced in U-U mice (P < 0.01). CONCLUSIONS: CUG results in increased adipose tissue lipogenic gene expression and adipocyte diameter but not increased cellularity, suggesting that catch-up fat is primarily associated with lipogenesis rather than adipogenesis in this murine model.
2009-05-14 | GSE16083 | GEO
Project description:Low (U) and normal (N) birth weight female porcine offspring were used to study molecular and physiological changes in the liver before and after postnatal feed restriction (R, 50% of controls) and after subsequent refeeding period in comparison to non-restricted control animals (K). Overall, the following questions were addressed at the transcriptional, epigenomic and metabolic level: 1) Are there differences in the hepatic transcriptional profile between U and normal birth weight 2) Are these effects reflected on the metabolic level? 3) Could the possible birth weight-dependent effects be modified through feed restriction intervention? 4) Are these effects persistent and, moreover, can improvements with regard to lipid homeostasis be observed? Microarrays were used to study the effects of birth weight and/or feed restriction on the transcriptional level.
2016-01-23 | GSE43826 | GEO
Project description:Mirobiota composition in low birth weight infants
| PRJDB10157 | ENA
Project description:We explored the hypothesis that gene expression will be dysregulated in the liver of low birth weight (LBW) offspring, distinct from normal birth weight (NBW) offspring, in young adulthood when both birth weight outcomes are challenged with a lifelong postnatal Western diet (WD). Independent of diet, in LBW vs. NBW males, 7 differentially expressed genes (DEGs) were identified, most of which downregulated (5 vs. 2) in LBW males. A similar trend was observed in LBW vs. NBW females, where 12 DEGs were identified, predominantly downregulated in the LBW group (9 vs. 3), irrespective of diet. Lifelong WD consumption exerted a marked influence on liver transcription profiles. Notably, 553 (444 upregulated and 109 downregulated) and 639 (533 upregulated and 106 downregulated) DEGs were identified in males and females, independent of birth weight, respectively. Additionally, in females, birth weight and WD both impacted six genes. Further, transcriptomic analysis revealed 22 (9 upregulated and 13 downregulated) and 55 (12 upregulated and 43 downregulated) DEGs between LBW/WD and NBW/WD groups in males and females, respectively.
2024-09-16 | GSE276971 | GEO
Project description:Stearoyl-CoA desaturase (SCD) is the rate-limiting enzyme catalyzing the conversion of saturated fatty acids palmitate and stearate to monounsaturated fatty acids palmitoleate and oleate. During adipocyte differentiation, SCD expression increases concomitantly with several transcription factors and lipogenic genes. We used microarrays to examine gene expression in differentiated pre-adipocytes treated with and without an SCD inhibitor. On day 7 of adipocyte differentiation, total RNA was extracted from adipocytes. Two conditions were selected for comparison: total RNA extracted from adipocytes treated with DMSO (control) and or a SCD inhibitor.
2014-04-04 | E-GEOD-51905 | biostudies-arrayexpress
Project description:Germline epigenetic programming, including genomic imprinting, substantially influences offspring development. Polycomb Repressive Complex 2 (PRC2) plays an important role in Histone 3 Lysine 27 trimethylation (H3K27me3)-dependent imprinting, loss of which leads to growth and developmental changes in mouse offspring. In this study, we show that offspring from mouse oocytes lacking the PRC2 protein Embryonic Ectoderm Development (EED) were initially developmentally delayed, characterised by low blastocyst cell counts and substantial growth delay in mid-gestation embryos. This initial developmental delay was resolved as offspring underwent accelerated fetal development and growth in late gestation resulting in offspring that were similar stage and weight to controls at birth. The accelerated development and growth in offspring from Eed-null oocytes was associated with remodelling of the placenta, which involved an increase in fetal and maternal tissue size, conspicuous expansion of the glycogen enriched cell population and delayed parturition. Despite placental remodelling and accelerated offspring fetal growth and development, placental efficiency and fetal blood glucose levels were low, and the fetal blood metabolome was unchanged. Moreover, while expression of the H3K27me3-imprinted gene and amino acid transporter Slc38a4 was increased, fetal blood levels of individual amino acids were similar to controls, indicating that placental amino acid transport was not enhanced. Genome-wide analyses identified extensive transcriptional dysregulation and DNA methylation changes in affected placentas, including a range of imprinted and non-imprinted genes. Together, while deletion of Eed in growing oocytes resulted in fetal growth and developmental delay and placental hyperplasia, our data indicate a remarkable capacity for offspring fetal growth to be normalised despite inefficient placental function and the loss of H3K27me3-dependent genomic imprinting.
2024-01-26 | GSE210398 | GEO